Evidence exists which implicates an immunologic mechanism in the pathogenesis of pulmonary fibrosis. A significant proportion of patients with pulmonary fibrosis have indications of autoimmune disease, such as rheumatoid factor, autoantibodies and the presence of a cell-mediated immune response to human type I collagen. Whether the immune response is a major contributor in the pathogenesis of pulmonary fibrosis or is just a secondary manifestation of lung injury is not known. The purpose of this proposal is to further and more directly investigate the role of the immune response in the development of bleomycin-induced pulmonary fibrosis in the rat. This will be accomplished by determining: 1) whether a local (lung) or systemic immune response to lung connective tissue (collagen types I and III) develops during the course of the disease, 2) with cell transfer experiments, if lymphocytes purified from lungs and spleens of animals with fibrotic lung disease will: a. localize in the lungs of normal recipient animals or in the lungs of recipient animals in which lung injury has been induced, or b. transfer fibrotic lung disease to normal recipient animals or recipient animals in which acute lung injury has been induced, 3) if immunization of animals (two groups - normal animals and animals in which during the course of immunization are induced with an agent which causes acute lung injury) to types I and III collagen will lead to lung injury, 4) if the development of the fibrotic lesion is altered in a T-cell depleted (thymectomized) animal. The significance of this proposal lies in its direct approach to analyze whether the immune system does or does not play an active role in the pathogenesis of pulmonary fibrosis. Whether or not evidence for an immune response is found in this experimental model, the data should nevertheless provide a better understanding of the diverse immunopathological parameters observed in pulmonary fibrotic diseases.